Ординатура / Офтальмология / Английские материалы / The Art and the Science of Cataract Surgery_Boyd, Barraquer_2000

Corticosteroids prevent the release of arachidonic acid from cell membranes, by blocking phospholipase A 2. Non steroidal antiinflammatory drugs are cyclo-oxygenase inhibitors, blocking the synthesis of prostaglandins.

Prophylactic Treatment

A randomized clinical trial by Flach et al demonstrated that cyclo-oxygenase inhibitors (COI) alone used prophylactically reduced the incidence of CME after cataract surgery. Ketorolac tromethamine 0.5% ophthalmic solution was administrated three times daily beginning one day before surgery and continued for 19 days postoperatively. Given the relatively low incidence of CME in uncomplicated cataract surgery, prophylactic treatment is seldom used.

Treatment of Chronic CME

Pooled data from randomized clinical trials indicate a treatment benefit in terms of improving final visual acuity by two or more lines. These studies report the efficacy of a combination of corticosteroid and cyclooxygenase inhibitors (COI, or NSAID's). In all but one trial, COI was tested alone with good results. Since there might be a synergistic effect, the following approach is suggested:

1. Topical corticosteroids, prednisone acetate 1% four times daily + topical COI (diclofenac sodium 0.1% or flurbiprofen sodium 0.03% or ketorolac tromethamine 0.5%) four times daily. The treatment is maintained at least for two months, with careful monitoring of the intraocular pressure. If the patient has a steroid pressure response, treatment

should be limited to topical COI. In case of favorable response, the regime is tapered very slowly. If there is no response at two months, the following interventions could be considered, without discontinuing the initial treatment.

2.Periocular steroid injections limited to a maximum of three.

3.Carbonic anhidrase inhibitors may work in a few patients but may be poorly tolerated.

4.Surgery should be considered only in patients with surgical complications that have modified the anatomy of the anterior segment and only if a well conducted pharmacological therapeutic trial has failed.

In patients with vitreous incarceration in the wound, Nd:YAG vitreolysis may be tried, but is difficult. An anterior vitrectomy, with repair of vitreous adhesion to the wound or iris may be the procedure of choice in these cases. More extensive surgery may be required if there is significant lens malposition.

Diabetes and Cystoid Macular

Edema

Verdaguer is an authority on diabetic retinopathy. He emphasizes once again that patients with preexisting diabetic macular edema are at substantial risk for worsening of the macular edema following cataract surgery. Moreover, diabetics are probably more susceptible to pseudophakic CME. The two conditions, diabetic macular edema and postsurgical CME may, in fact, coexist in a given diabetic patient. Patients with lipidic exudates, retinal hemorrhages, perifoveal microaneurysms, diffuse or focal leakage at angiography will have a predominantly diabetic macular edema. Patients without these characteristics, a petaloid pattern of leakage

at the macula, and disc leakage, will have a predominantly postsurgical CME.

Treatment Recommendations

1.Optimize medical treatment. (metabolic control, arterial hypertension, dislipidemia, anemia).

2.Use topical steroids and COI, to treat the presumed pseudophakic CME.

3.Laser photocoagulation, focal or grid, if there are leaking microaneurysms or diffuse leakage, with lipid exudation and retinal hemorrhages.

PHOTIC MACULOPATHY

The intense illumination system of modern operating microscopes may induce photochemical retinal injury. The first cases of phytotoxicity after uneventful cataract surgery were described by McDonald and Irvine (1983).

Photochemical vs Photothermal Damage

Verdaguer clarifies that photochemical injury is different from photothermal damage (photocoagulation). Photocoagulation occurs after brief and intense light exposure; photochemical injuries develops after prolonged exposure at intensity too low to induce photocoagulation. Photocoagulation induces an immediate visible reaction; photochemical damage is not immediately recognizable.

In photochemical injuries, light activation of cell molecules generates oxygen singlets (free oxygen radicals). These are very toxic and induce oxidation and damage of cell components.

Shorter wavelengths carry most energy (UV and blue visible light) and are more likely to produce photochemical damage.

Incidence

Juan Verdaguer points out that the incidence of photoretinal injuries during extracapsular cataract surgery has been estimated at 7 to 28% in different series. Photic retinal injury did not develop after phacoemulsification in one series, with careful limiting of coaxial exposure time and microscope irradiance.

Risk Factors

The main risk factors associated with photochemical damage are duration of the exposure (longer surgery time) and intensity of the operating microscope illumination.

Longer surgery times have been associated with increased incidence of retinal photochemical injuries. However, the complication has occurred in short, uneventful procedures. Therefore, the skilled, rapid, experienced surgeon, should not disregard the dangers of photoxicity.

Clinical Findings

The patient may complain of a scotoma that may be central or paracentral, in correspondence to the retinal injury location. A few patients may give a history of postoperative erithropsia. In other cases the main complaint may be unexpected poor visual acuity, if the injury is near the fovea.

Visible changes at the retina will be apparent 24 to 48 hours following exposure. In the early postoperative period the lesion appears a subtle creamy deep, pale oval lesion, usually just below or above or temporal

to the center of the fovea. If the eye is infraducted by a superior rectus suture, the lesion will be located below the macula.

Fluorescein angiography will show intense staining of the oval plaque. Cicatricial changes are apparent within the first week, with pigmentary mottling and athropic changes of the pigment epithelium within a sharply demarcated oval area. The lesion shows a highly characteristic leopard-skin appearance.

The scotoma fades rapidly and the visual acuity may improve, unless the lesion is large and involves the macula. Fluorescein angiography will reveal changes restricted to the oval scar, with window defects and blocked fluorescence corresponding to the areas of hyperpigmentation (Fig. 159).

Preventive Measures

The illuminating light should not be brighter than necessary and the cornea should be covered whenever the surgeon is not working intraocularly. A finger blocking the light may suffice.

Indirect illumination, instead of coaxial illumination should be used during closure of surgical wound in extracapsular procedures, since the risk is maximal following implantation of the lens, with the light clearlu focused directly on the retina.

Tilting the microscope toward the surgeon and infraduction of the globe may displace the light below the fovea.

Small incision phacoemulsification technique is less likely to induce light toxicity, since the instruments remain in the visual axis most of the time and operating times are reduced in the hands of experienced surgeons. There is no treatment for this complication.

Photosensitizing agents, such as hidroxchloroquine,phenotiazines, allopurinal, etc., should be discontinued before surgery, since they may potentiate photic damage to the retina.

AMINOGLYCOSIDE TOXICITY

Aminoglycosides have been widely used in the prophylaxis and treatment of ocular infections. Macular infarction is a severe complication that has been mainly associated with the administration of gentamicin, but has also been reported after use of amikacin and tobramycin.

Juan Verdaguer emphasizes that aminoglycoside toxicity may be related to:

1) Intravitreal injections in endophthalmitis treatment regimes. Toxicity may follow administration of gentamicin at recommended doses. Verdaguer has seen this complication after intravitreal injection of 0.15 mg of gentamicin, a dose previously considered safe.

Treatment of post surgical endophthalmitis should include the intravitreous injection of an antibiotic which acts effectively against gram-positive organisms (vancomycin) and one that is effective against gram negatives, since gram-negative endophthalmitis is much more common. Given the very narrow safe therapeutic window of aminoglycosides, a good choice would be a cephalosporin such as ceftazidime. If the surgeon is confronted with an acute postsurgi-

cal endophthalmitis and ceftazidime is not available, an aminoglycoside should be included in the intravitreous injection, at the lowest effective dose (100 mg of gentamicin or 400 mg of amikacin). Even at these doses, toxicity cannot be ruled out.

2)Prophylactic intravitreous injections in severe trauma cases. Verdaguer has seen this complication after a prophylactic intravitreous tobramycin injection.

Aminoglycosides should not be used intravitreally for prophylactic purposes.

Endophthalmitis is a treatable disease and aminoglycoside toxicity is not. (Campochiaro et at).

3)Following uncomplicated subconjunctival injection after routine cataract surgery. Although this has been reported in the literature, Verdaguer has never seen a case. The complication is believed to be associated with leakage of the antibiotic into the eye through the cataract wound (with or without sutures). The tunnelled, non-sutured wounds, create a one way valve, allowing subconjunctival antibiotics and access into the anterior chamber. Subconjunctival antibiotic injections, if used, should be placed in the quadrant opposite to the wound.

4)Dilution errors in intravitreal injec-

tions.

5)Inadvertent intraocular injection due to confusion with miochol or other substances. If the mistake is discovered during surgery, profuse anterior segment lavage should be done, immediately. Immediate vitrectomy has also been recommended.

Clinical Findings

Vision is profoundly affected the day following surgery or the intravitreal injection. Usually, the retinal infarction affects the

macular area. (Intravitreal aminoglycosides tend to settle on the posterior pole in the supine position). Examination reveals milky white opacification of the retina, a cherry red spot and a few blot retinal hemorrhages. The appearance is similar to that seen in central retinal artery occlusion, but limited to the posterior pole. It also differs from branch retinal arterial occlusion, since the infarction involves the retina both above and below the macula. Fluorescein angiography reveals sharply demarcated central area of occlusion of the retinal vessels and some perivascular leakage (Fig. 160).

Figure 160: Aminoglycoside Toxicity 2 Months after Intravitreous Injection of Gentamicin

Vascular occlusion involving the temporal vessels (Macular infarction). (Courtesy of Prof. Juan Verdaguer, M.D.)

The condition is untreatable and irreversible. Optic atrophy and atrophic and pigmentary retinal changes develop later.

POSTERIOR CAPSULE OPACIFICATION

Overview

Okihiro Nishi, M.D., is a renowned authority on this subject because of his extensive research and revealing findings. Nishi has emphasized that posterior capsule opacification (PCO) is the most frequent postoperative complication associated with decreased vision in cataract surgery. Itoccurs with an incidence of up to 50% within 5 years after surgery.

Various mechanical, pharmaceutical and immunologic techniques have been applied in attempts to prevent PCO by removing or killing residual lens epithelial cells

(LECs), but none has been confirmed to be satisfactorily practical, effective and safe for routine clinical practice. Nishi emphasizes that the most effective approach to reduce or delay the incidence of PCO is by inhibiting the migration of LECs and not by killing the cells.

Main Causes of PCO

Recent clinical, pathological and experimental studies have emphasized that PCO is usually secondary to a proliferation and migration of residual lens epithelial cells. (LECs).

How LECs Invade the Posterior

Capsule

Nishi has pointed out that residual LECs proliferate at the pre-equatorial germinative zone and migrate posteriorly onto the posterior capsule postoperatively. In addition, when the anterior capsule comes into contact with the posterior capsule, the LECs underneath the anterior capsule also migrate onto the posterior capsule abundantly, before the two capsules adhere and grow together. The apposition of the anterior capsule and the posterior capsule can induce fibrotic PCO.

Role of IOL in PCO

When the IOL is in the capsular bag the optic can separate both capsules, and interferes with the LEC migration from the anterior capsular edge onto the posterior capsule. The inhibition of migrating LECs and the separation of the capsules by the IOL optic are the main reasons why the incidence of PCO is significantly lower in eyes with an IOL than in those without one.

Specific Features of the AcrySof

and PCO

Nishi points out that the AcrySof IOL reportedly has a significant low incidence of PCO. His recent studies indicate that this effect may be due to the sharp and rectangular edge design of the AcrySof IOL. His histopathologic findings of the lens capsule con-

taining an AcrySof IOL in rabbits disclose that the lens capsule wrapped the IOL so firmly that it conformed faithfully to the rectangular sharp optic edge of the IOL and that migrating LECs were apparently inhibited at this capsular bend or angle created by the sharp edge and posterior capsule by contact. The creation of such a bend or angle in the posterior capsule requires a well-centered CCC, smaller than the IOL optic, so that the CCC edge is in apposition to the optic.

On the other hand, the role of this lens may be dependent not only on the rectangular edge design but also on the features of the IOL acrylic material, such as adhesiveness. The AcrySof IOL has triple the adhesiveness to a collagen film compared to a PMMA IOL. The adhesiveness may also help to facilitate the creation of the bend. Moreover, the acrylic material itself may have effects on the inhibition of migrating LECs. This adhesiveness property of the acrylic lens, which we described as "tackiness" in Chapter 9 under "Advantages and Properties of Acrylic Lenses" merits further investigation. This "tackiness" or adhesiveness seems to play a role in the positive effects of the AcrySof lens. If so, then this might be a factor of particular importance for the use of acrylic lenses and designs of future IOL's.

From the analysis provided here, it is clear that the preventive effect on PCO of an AcrySof IOL may be both design and material dependent.

Role of Continuous Curvilinear

Capsulorhexis in PCO

Nishi emphasizes that continuous curvilinear capsulorhexis (CCC) can contribute to reduce PCO because it facilitates the implantation of an IOL symmetrically in the capsular bag maintaining it there without decentration. It is extremely important to create a well-centered CCC of the correct size for the prevention of migrating LECs. The CCC edge should be smaller than the IOL optic and cover its margin (Fig. 145). A decentered, oversized CCC or incomplete CCC with a radial tear (Fig. 146) may result in the apposition of both capsules. Even though the defective area lies in a very limited circumference, the LECs migrate from the edge of the anterior capsule onto the posterior capsule, causing PCO.

Main Factors that Reduce PCO

Nishi clarifies that there are three key factors that play an important role in reducing the incidence of PCO: 1) the design of the IOL, which results in the creation of a sharp bend in the capsule. The discontinuous, rectangular bend or angle in the posterior capsule interferes with the proliferation of LECs. 2) The material of the IOL, which points to the benefits of some acrylic because of its adhesive properties and biocompatibility (less fibrosis). 3) The surgical technique which emphasizes a perfectly

centered CCC of smaller size than the IOL optic.

In addition, Nishi strongly recommends a NSAID for 3 months postoperatively, in order to reduce postoperative inflammation with conversion of mononuclear cells into fibroblasts, and possibly proliferation of residual LECs.

Visual Loss from PCO - Differential Diagnosis

It is often a rather difficult clinical judgment to determine if the capsule opacity is in fact responsible for the patient`s decreased vision. The principal misdiagnosis is to believe that the capsule is responsible for the problem when, in fact, the patient has developed a cystoid macular edema which may be difficult to detect because of the posterior capsular opacity. When in doubt, a pre-capsulotomy fluorescein angiography is appropriate to determine if macular edema is present.

PERFORMING THE POSTERIOR CAPSULOTOMY

Size of Capsulotomy

Some prestigious anterior segment surgeons have advocated not dilating the pupil for performing a YAG posterior capsulotomy. Many patients' pupillary openings are not located in the exact anatomical center of the iris. Once the pupil is dilated, it can be difficult to identify where the true pupillary opening was located.

Nevertheless, there are important contraindications to making a small capsulotomy. The most important are: 1) Difficulties in the evaluation of the retinal fundus. 2) The center of the capsulotomy may be clear following treatment but the rest of the capsule remains opaque, and sometimes with a crystalloid appearance. Patients with macular degeneration, for example, may see better when the capsulotomy is wide enough to prevent contrast reducing haze from the residual hazy peripheral capsule. In those cases it is better to dilate the pupil 4-5 mm preoperatively in order perform a more effective treatment.

Dodick generally makes a capsule opening the size of a normal pupil, 3-4 mm at the most.

Posterior Capsulotomy Laser

Procedure

Timing

Alice McPherson, M.D., was one of the first retina specialists to demonstrate that retinal detachment could be precipitated by early YAG laser posterior capsulotomy. She has advised waiting approximately 4-6 months after cataract surgery to perform a YAG laser posterior capsulotomy. The prior dictum to wait one year, was done to be sure all inflammation was finished, in order to avoid cystoid macular edema.

McPherson has pointed out that once a capsulotomy is performed, the pseudophakic eye is actually like an aphakic eye. Keeping the patient`s posterior lens capsule in place as

long as possible can reduce the tendency for vitreous traction on the periphery. After the YAG capsulotomy is done, any predisposing factor can increase the potential for a retinal detachment or cystoid macular edema.

Technique

Use the lowest level energy pulse that will open the capsule, usually 1 mJ. An

adequate opening can be made with 10 laser applications or less, depending on how taught the capsule is. A cruciate pattern is recommended, starting in the periphery at 12 o'clock, working down across the center of the capsule toward 6 o'clock, and complete the cross from 3 to 9 o'clock (Fig. 161). The capsule will usually retract further after completing the capsulotomy.

Complications Following Nd:YAG

Posterior Capsulotomy

Intraocular Pressure Elevation

The most common complication is a transient pressure elevation. This must be anticipated and treated prophylactically. The most effective method is to instill one drop of brinzolamide or dorzolamide 30 minutes before and one drop following the laser procedure. Patients at higher risk of developing transient elevation of the intraocular pressure are those that have anterior chamber intraocular lenses and patients with pre-existing glaucoma.

Retinal Detachment

A higher percentage of pseudophakic detachments occurs in cases with a history of fellow eye detachment, preexisting retinal disease such as lattice degeneration and retinal holes, or in eyes with axial lengths above 25 mm. Retinal detachments associated with Nd:YAG laser posterior capsulotomy occur most often within the first 6 months following capsulotomy.

Cystoid Macular Edema

It is not well-known yet whether Nd:YAG laser capsulotomy can induce the formation of cystoid macular edema (CME) in a quiet eye. Anterior segment inflammation can occur after laser capsulotomy, and inflammation has been identified as an etiologic factor for CME especially if laser treatment has been more intensive than the parameters already established. In addition, prolapse of vitreous anteriorly through the capsu-

lotomy or a disruption of the anterior hyaloid might produce posterior retinal traction, another possible cause for CME. Thus, a potential relationship does exist. In suspicious cases only a fluorescein angiogram after the treatment may provide the answer.

POSTOPERATIVE ASTIGMATISM IN CATARACT PATIENTS

With present advances in small incision cataract surgery, particularly with clear corneal incisions, postoperative astigmatism following phacoemulsification should be minimal. A well trained surgeon creates an astigmatically neutral incision to prevent an induced astigmatism.

If astigmatism is present preoperatively, the surgeon addresses the problem at the time of cataract surgery. By placing the corneal incision in the indicated axis, preexisting astigmatism and cataract surgery are performed simultaneously. This latter subject which we term "Refractive Cataract Surgery" is addressed at the beginning of Chapter 12 (Cataract Surgery in Complex Cases).

MANAGEMENT

Astigmatism, either preexisting that was not fully corrected or induced may be managed after cataract surgery either with incisional refractive surgery (astigmatic keratotomy) or with excimer laser (LASIK or PRK).

How to Proceed

Wait a minimum of three months following surgery in order to deal with a stable